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. 2022 Aug 1;61(3):112. doi: 10.3892/ijo.2022.5402

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Copyright: © Zhang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Overexpression of HHLA2 promotes the proliferation, migration and invasion of GBC in vitro whilst promoting tumor formation in vivo. (A) Wound healing assay and (B) subsequent quantification showed that HHLA2 overexpression enhanced cell migration. Scale bars, 100 µm. (C) HHLA2 overexpression was found to increase invasive capability, (D) which was quantified. Scale bars, 100 µm. (E) The proliferative abilities of the cells overexpressing HHLA2 were higher compared with those of the HLLA2-NC group, (F) according to the quantification. Scale bars, 100 µm. Green, EdU; Blue, DAPI. (G) Representative images of mice in each group harboring the tumors. (H) Overexpression of HHLA2 increases the diameters and the weights of GBC tumors according to the mouse xenograft assay, (I) which was qualified (n=6). ^**P<0.01 and ^***P<0.001 (HHLA2 group vs. HHLA2-NC group). HHLA2, human endogenous retrovirus-H long terminal repeat-associating protein 2; GBC, gall bladder cancer; NC, negative control.